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Biomedical subjects

E Goldstein

Publications and source records attributed to E Goldstein.

At least 145 records · Page 8Linked to original sources
PubMed1973

Role of immunity in viral-induced bacterial superinfections of the lung.

Although viral illnesses are predisposing causes for pulmonary bacterial infections, the interrelationships of viral virulence and host immunity to alterations in susceptibility to bacterial infection are incompletely understood. We used two mutant strains of encephalomyocarditis virus (minimally virulent Mengo-37A and a highly virulent Columbia SK [Col-SK]) to investigate these interrelationships. Mice that had been immunized to Mengo-37A, and nonimmunized controls, were challenged with aerosols containing 10(4) plaque-forming units of Mengo-37A or Col-SK per liter. The effect of each viral infection on pulmonary antibacterial activity was assessed 3 days later by measuring the capacity of the lungs to kill inhaled radiophosphorus ((32)P)-labeled Staphylococcus aureus. The degree of antibacterial dysfunction found was proportional to the virulence of the infecting virus. If the host was immune to the infecting virus, bactericidal function was not impaired by viral challenge. Neither mutant caused significant pulmonary damage; therefore: (i) viral-induced impairment in bactericidal activity reflects, quantitatively, the virulence of the virus and (ii) viral immunity protects pulmonary bacterial defenses by preventing damage to the phagocyte from the virus or its attendant metabolic abnormalities.

Aerosols↗
PubMed1972

Murine resistance to inhaled Neisseria meningitidis after infection with an encephalomyocarditis virus.

A reduction in pulmonary anti-bacterial activity due to a preceding viral illness has been suggested as the mechanism responsible for some meningococcal infections of the lung. We investigated this proposed pathogenesis by infecting mice with airborne encephalomyocarditis virus (EMC) and then challenging them 1, 4, and 7 days later with aerosols of Neisseria meningitidis. Meningococcal clearance was assessed by comparing the numbers of bacteria present immediately after inhaling the aerosols with the numbers present 3 hr later. To insure that EMC virus adequately depressed murine defense mechanisms, we also determined staphylococcal killing rates at 4 hr by using radiophosphorus-labeled staphylococcal aerosols. Viral infection depressed murine pulmonary antimeningococcal activity at 1 and 4 days (P < 0.01) but not at 7 days. Intrapulmonary staphylococcal killing was impaired on day 4 (P < 0.01) but not on days 1 or 7. Pulmonary viral titers decreased rapidly from 10(7) to 10(3) plaque-forming units/ml of lung during the experimental period. According to these data viral disease transiently depresses resistance to meningococcal infection. This impairment in host resistance is present while the viral titer is decreasing and follows a relatively similar pattern to the transient decrease noted for staphylococci.

Aerosols↗
PubMed1971

In vitro chemotherapeutic combinations against isoniazid-resistant Mycobacterium tuberculosis and Mycobacterium fortuitum.

It is an acceptable medical practice to use second-line antimycobacterial drugs in combination with isoniazid in treatment of isoniazid-resistant tuberculosis. Recent investigations have demonstrated the importance of determining chemotherapeutic interaction in instances of multiple antibiotic use. We studied the inhibitory effect of combinations of isoniazid with ethambutol, rifampin, ethionamide, cycloserine, viomycin, and kanamycin against three isoniazid-resistant strains of Mycobacterium tuberculosis and three strains of M. fortuitum. The isobologram technique with drug concentrations of 0.4 to 100 mug/ml was used. With the exception of single instances in which kanamycin plus isoniazid (M. tuberculosis strain 9999) and ethionamide plus isoniazid (M. fortuitum strain 2080) seemed to have a synergistic effect, neither synergy nor antagonism was noted for any of the combinations. These studies show that the combined use of isoniazid and a second line antimycobacterial agent results in vitro in indifferent inhibitory activity.

Antitubercular Agents↗